Cardiovascular risk is directly linked to sleep related breathing disorders (SRBD). The number of U.S. laboratories that study sleep, roughly 2,792, is incredibly low when compared to the number of Americans estimated to have a chronic SRBD, just over 40 million. The average number of beds per lab is 3.6 bringing the total number of beds in which to do a sleep study to roughly 10,000. This means that to test all 40 million Americans, there would be 4,000 patients that would be seen per bed. If sleep tests were run 365 days per year, the result is an astounding 11 years of conclusive tests needed to be run to test the current population of individuals suffering form SRBD. The length of time increases as one considers the actual number of days per year sleep labs actually test patients, plus the amount of tests that need to be re-run due to inconclusive testing, plus the number of patients that continually need to be retested to see if their treatment is functioning properly. Given this scenario, it is no shock that wait times for patients to be scheduled for a sleep test can typically range from six weeks to six months. The problem will only increase, as “it is estimated that nearly 80 million Americans will have a sleep problem by the year 2010 and 100 million will have one by the year 2050.” Clearly then, the problem with wait time for testing should be addressed immediately to relieve pent up demand.
The current “gold standard” for testing sleep related breathing disorders is full polysomnography. Full polysomnography is, however, quite labor intensive, requires considerable instrumentation and is therefore rather expensive to conduct. As a result, many sleep laboratories have found it difficult to keep up with the demand for this test, and a long waiting list becomes the norm. Given that obstructive sleep apnea (OSA) is quite prevalent, leads to serious complications and that treatment options exist, it is important that individuals suffering from the disease are identified.
The need to study the ANS has been realized in academia for a considerable time. It is known in the field of microneurography that rapid-eye movement (REM) sleep is associated with profound sympathetic activity. It has also been found that arousals from non-rapid-eye movement (NREM) elicits K complexes that are associated with sympathetic activity. The sympathetic division of the ANS prepares a body for movement. Arousals require movement and hence an arousal requires sympathetic activation.
Generally, patients with OSA, a type of SRBD, have extremely disrupted sleep and terribly high daytime somnolence. Obstructive sleep apnea events are always accompanied by an acute rise in systolic blood pressure (rises in systolic blood pressure are associated with sympathetic activation), even when the usual EEG criteria for arousals are not met (a recognizable cortical electroencephalographic arousal). The duration of the apnea of individuals that demonstrate EEG arousal and those that do not meet the usual criteria for defining an arousal have been found to be identical. The pleural pressure peak, at the end of apnea, is identical between the two types of arousals, as are the EEG frequencies. These findings suggest that monitoring the cardiac changes of sleep is a more accurate measurement.
It has been demonstrated that apneic episodes result in progressive increases in sympathetic nerve activity. The increases are most marked toward the end of the apnea, when a patient moves. These findings are exactly what is excepted of sympathetic activation and its relationship to arousals in patients with SRBD.
Because cardiovascular control during sleep is primarily dictated by brain states that produce profound variation in ANS activity, many studies have been conducted to monitor the ANS. Since the data shows clearly that monitoring the ANS or cardiac changes in sleep yields more accurate data defining an arousal in sleep, it is clear that diagnostic studies must include ANS or cardiac monitoring.
It has been shown that in transitions from NREM to REM sleep, heart rate accelerations precede the EEG arousals marking the onset of REM. Therefore, not only does monitoring ANS activity give the clinician a possibly more accurate study, but also changes in ANS activity precede that information being observed via the EEG electrodes.
There are two existing technologies that attempt to monitor the ANS, namely pulse transit time (PTT) and peripheral arterial tonometry (PAT). Neither PTT nor PAT can lay claim to monitoring the ANS without adding additional sensors. PTT requires the use of ECG electrodes that may be difficult for a patient to self-apply due to skin cleaning and shaving requirements. PAT requires a very costly gauntlet-type device with a single-use finger pressure cuff. Also, the addition of extra sensors adds to noise artifact and difficulty in patient use. It is therefore an object of the present invention to provide an improvement over existing PTT and PAT technology through a more economical and more easily used device without need of additional sensors.
Several disclosures have been made in the prior art that teach methods and devices for diagnosis and monitoring of sleep breathing disorders using physiological data obtained from pulse oximetry-derived waveforms.
U.S. Pat. No. 5,398,682 to Lynn (Mar. 21, 1995) discloses a method and apparatus for the diagnosis of sleep apnea utilizing a single interface with a human body part. More specifically, a device is disclosed for diagnosing sleep apnea by identifying the desaturation and resaturation events in oxygen saturation of a patient's blood. The slope of the events is determined and compared against various information to determine sleep apnea.
U.S. Pat. No. 6,363,270 B1 to Colla, et al. (Mar. 26, 2002) discloses a method and apparatus for monitoring the occurrence of apneic and hypopneic arousals utilizing sensors placed on a patient to obtain signals representative of at least two physiological variables, including blood oxygen concentration, and providing a means for recording the occurrence of arousals. Obtained signals pass through conditioning circuitry and then processing circuitry, where correlation analysis is performed. A coincident change in at least two of the processed signals are indicative of the occurrence of an arousal that in turn indicates an apneic or hypopneic episode has occurred. A patient thus can be diagnosed as suffering conditions such as obstructive sleep apnea.
U.S. Pat. No. 6,529,752 B2 to Krausman and Allen (Mar. 4, 2003) discloses a method and apparatus for counting the number of sleep disordered breathing events experienced by a subject within a specified time period. Such a counter comprises: (1) an oxygen saturation level sensor for location at a prescribed site on the subject, (2) an oximetry conditioning and control module that controls the operation of the sensor and converts its output data to oxygen saturation level data, (3) a miniature monitoring unit having a microprocessor, a memory device, a timer for use in time-stamping data, a display means and a recall switch, and (4) firmware for the unit that directs: (i) the sampling and temporary storage of the oxygen saturation level data, (ii) the unit to analyze using a specified method the temporarily stored data to identify and count the occurrence of the subject's disordered breathing events, and to store the time of occurrence of each of these events, and (iii) the display means to display specified information pertaining to the counts in response to the actuation of the recall switch.
U.S. Pat. No. 6,580,944 B1 to Katz, et al. (Jun. 17, 2003) discloses a method and apparatus for identifying the timing of the onset of and duration of an event characteristic of sleep breathing disorder while a patient is awake. Chaotic processing techniques analyze data concerning a cardiorespiratory function, such as oxygen saturation and nasal air flow. Excursions of the resulting signal beyond a threshold provide markers for delivering the average repetition rate for such events that is useful in the diagnosis of obstructed sleep apnea and other respiratory dysfunctions.
The above references all make use of oxygen saturation data obtained through pulse oximetry to determine arousals and/or sleep breathing disorders. Each necessarily requires additional analysis and calculation of blood oxygen concentrations in order to render information useful specifically in the diagnosis and monitoring of sleep breathing disorders. It is therefore another object of the present invention to provide a more simplified method of obtaining and analyzing physiological data that accurately represents ANS activity.